2  ways  to  treat  a  fracture-­‐    1.  Closed  (external)  reduction:the  doctor  manipulates  the  bone  into  position.    2.  Open  (internal)  reduction  is  secured  by  a  surgery  procedure  involving  pins  or  wires  

   

HOMEOSTATIC  IMBALANCES  OF  BONE  AND  JOINTS    

Disease   Cause   Who  it  affects   Symptoms  RICKETS   caused  by  lack  

of  calcium  or  Vita  D.  

 disease  in  children;  

bowed  legs,  deformities  of  the  pelvis,  skull  and  rib  cage  are  common.  Epiphyseal  plates  are  not  calcified  and  widen,  ends  of  long  bones  become  enlarged.    

OSTEOPOROSIS   bone  resorption  (osteoclast)  is  faster  than  bone  deposit  (osteoblast)  

 disease  in  the  elderly;  

Bones  become  fragile  by  being  porous  and  light.  Spongy  bone  in  the  spine  most  vulnerable,  but  also  affects  the  entire  skeleton.  

OSTEO  ARTHRITIS  

Inflamed  or  damage  to  the  joints  

disease  in  the  elderly;  most  common,  occurring  in  more  women  than  men  

‘wear  and  tear’  arth.;  articular  cartilage  break  down  and  is  destroyed  faster  than  replaced  

RHEUM.  ARTHRITIS  

  Ages  30-­‐50;  autoimmune     Joint  tenderness  and  stiffness  in  the  synovial  joints  

GOUTY  ARTHRITIS  

Blood  levels  have  uric  acid  (urine)  which  form  into  crystals  in  the  joints  

Common  in  men  over  women  because  they  have  higher  blood  levels  of  uric  acid;  inherited  disease  

Untreated  gout  can  be  destructive;  articulating  bone  ends  fuse  and  immobilize  the  joint.  Treatment  :  meds  prevent  gout  attacks.  Must  drink  water  and  avoid  alcohol  excess  

   

Chapter 6 Bones and Skeletal Tissues 189

6begin cleaning up the debris. Meanwhile, fibroblasts andosteoblasts invade the fracture site from the nearby perios-teum and endosteum and begin reconstructing the bone.The fibroblasts produce collagen fibers that span the breakand connect the broken bone ends, and some differentiateinto chondroblasts that secrete cartilage matrix. Within thismass of repair tissue, osteoblasts begin forming spongybone, but those farthest from the capillary supply secretean externally bulging cartilaginous matrix that later calci-fies. This entire mass of repair tissue, now called thefibrocartilaginous callus, splints the broken bone.

Bony callus forms. Within a week, new bone trabeculaebegin to appear in the fibrocartilaginous callus and graduallyconvert it to a bony (hard) callus of spongy bone. Bonycallus formation continues until a firm union is formedabout two months later.

Bone remodeling occurs. Beginning during bony callus for-mation and continuing for several months after, the bonycallus is remodeled. The excess material on the diaphysisexterior and within the medullary cavity is removed, andcompact bone is laid down to reconstruct the shaft walls.The final structure of the remodeled area resembles that ofthe original unbroken bony region because it responds tothe same set of mechanical stressors.

C H E C K Y O U R U N D E R S TA N D I N G

19. If osteoclasts in a long bone are more active thanosteoblasts, what change in bone mass is likely?

20. Which stimulus—PTH (a hormone) or mechanical forces act-ing on the skeleton—is more important in maintaining ho-meostatic blood calcium levels?

21. How does an open fracture differ from a closed fracture?22. How do bone growth and bone remodeling differ?

For answers, see Appendix G.

4

3

Homeostatic Imbalances of Bone! Contrast the disorders of bone remodeling seen in osteo-

porosis, osteomalacia, and Paget’s disease.

Imbalances between bone deposit and bone resorption underlienearly every disease that affects the adult skeleton.

Osteomalacia and RicketsOsteomalacia (os!te-o-mah-la!she-ah; “soft bones”) includes anumber of disorders in which the bones are inadequately min-eralized. Osteoid is produced, but calcium salts are not de-posited, so bones soften and weaken. The main symptom is painwhen weight is put on the affected bones.

Rickets is the analogous disease in children. Because youngbones are still growing rapidly, rickets is much more severe thanadult osteomalacia. Bowed legs and deformities of the pelvis,skull, and rib cage are common. Because the epiphyseal platescannot be calcified, they continue to widen, and the ends of longbones become visibly enlarged and abnormally long.

Osteomalacia and rickets are caused by insufficient calciumin the diet or by a vitamin D deficiency. For this reason, drink-ing vitamin D–fortified milk and exposing the skin to sunlight(which spurs the body to form vitamin D) usually cure thesedisorders. Although the seeming elimination of rickets in theUnited States has been heralded as a public health success, rick-ets still rears its head in isolated situations. For example, if amother who breast-feeds her infant becomes vitamin D defi-cient because of dreary winter weather, the infant too will bevitamin D deficient and will develop rickets.

OsteoporosisFor most of us, the phrase “bone problems of the elderly”brings to mind the stereotype of a victim of osteoporosis—ahunched-over old woman shuffling behind her walker.

1 A hematoma forms. 2 Fibrocartilaginous callus forms.

3 Bony callus forms. 4 Bone remodeling occurs.

Figure 6.15 Stages in the healing of a bone fracture.